Cardio. Cardiogenic Shock. Chap 39 ACVIM MMVD Flashcards

1
Q

Cardiogenic shock is defined as

A

inadequate cellular metabolism secondary to cardiac dysfunction, despite adequate intravascular volume

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2
Q

Clinical signs are consistent with:

A

global hypoperfusion

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3
Q

Systolic or diastolic dysfunction or arrhythmias can result in decreased stroke volume, forward flow failure, and cardiogenic shock…
most common cause of systolic dysfunction:

A

dilated cardiomyopathy

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4
Q

Systolic dysfunction secondary to mechanical failure is less common.. examples:

Diastolic dysfunction can occur secondary to:

Severe bradyarrhythmias:

A

subaortic stenosis
hypertrophic obstructive cardiomyopathy
acute mitral regurgitation secondary to ruptured chordae tendineae

cardiac tamponade
hypertrophic cardiomyopathy
tachyarrhythmias

third-degree atrioventricular block
sick sinus syndrome can lead to a severe decrease in cardiac output and thus cardiogenic shock

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5
Q

The normal physiologic response to a decrease in stroke volume is a compensatory increase in heart rate (and systemic vascular resistance) to maintain
cardiac output. This is mediated by:

A

baroreceptor-mediated sympathetic

stimulation

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6
Q

In response to cardiac dysfunction–induced hypotension, neurohormonal mechanisms (e.g., renin-angiotensin-aldosterone system) increase the effective circulating volume .:. forward failure in patients with chronic cardiac conditions is _____

A

rare, most patients detriorate secondary to the increase in preload and subsequent congestive (backward) heart failure and pulmonary edema

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7
Q

Some patients may suffer from concurrent forward and backward failure ie.

Patients that demonstrate an acute decrease in cardiac output do not have time to compensate:

A

DCM

ruptured cordae, tamponade
right-sided backward failure (e.g., ascites).

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8
Q

diagnosis of cardiogenic shock

A

difficult - CS consistent with global hypoperfusion: depression, unresponsiveness, or disorientation. Peripheral extremities will be cold, CRT, pale

ECG, CXR, ECHO, BP

Even with advanced diagnostic imaging, the diagnosis of cardiogenic shock can still be difficult

A pulmonary arterial catheter -
decreased CO, increase in the preload CVP, PAP and PAWP

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9
Q

Endomyocarditis

A

rare condition of cats
-several days after a routine procedure such as neutering -normal myocardial function before the anesthesia and the procedure is usually uneventful, but cardiac dysfunction, hypotension, pulmonary edema, and interstitial pneumonia rapidly develop
-not well described, the endocardium is hyperechoic on
echocardiography, and histopathology reveals neutrophilic inflammation and fibroplasia

-positive pressure ventilation the prognosis is often poor.

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10
Q

Tamponade, explain what type of cardiac dysfunction is occuring:

A
  • diastolic dysfunction
  • decreased diastolic ventricular filling will lead to a decrease in SV and CO
  • in an attempt to maintain normotension and tissue perfusion, a reflex tachycardia will ensue
  • eventually the increase in heart rate will not be sufficient to maintain an adequate CO and patient will become hypotensive
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11
Q

pseudohypoadrenocorticism

A

If the effusion is chronic, the patient may have decreased sodium and increased potassium bc reduced effective circulating volume–induced pseudohypoadrenocorticism.

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12
Q

Tamponade and fluids?

A

systemic manifestations of this condition result from the decreased preload, increasing intravascular volume with a fluid bolus is warranted.

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13
Q

Why give all second-degree AV block atropine:

A
  • can be vagally mediated or secondary to sinoatrial or AV nodal pathology
  • atropine response test (0.02 to 0.04 mg/kg intravenously [IV]) is warranted in all cases
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14
Q

Sepsis cardiogenic shock

A

rare - usually hyperdynamic
-reduction in ventricular compliance, biventricular dilation, and decrease in contractile function all decrease EF

Myocardial dysfunction peaks 1-3 days of sepsis
shown to resolve w.in 7 to 10 days in patients who survive

Low cardiac output is rare in patients with
septic shock but often is due to end-stage decompensated

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15
Q

chronic Stage C

alternative to lasix.
dose:
frequency:

A

PO furosemide administration to effect, commonly at a dosage of 2 mg/kg administered q12h

torsemide at 1/10‐1/20 or approximately 5% to 10% of the furosemide dosage, or approximately 0.1‐0.3 mg/kg q24h

pimobendan, an ACEI, and spironolactone

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16
Q

what pushes stage C to D?

A

Chronic PO furosemide dosages ≥8 mg/kg q24h (or the equipotent torsemide dosage) + pimobendan, an ACEI, and spironolactone indicate disease progression to Stage D

17
Q

causes of diuretic resistance

A
noncompliance (ie, not receiving the drug)
high sodium intake
slow absorption (eg, gut edema) 
impaired secretion into the renal tubular lumen (eg, chronic kidney disease, advanced age, concurrent NSAID)
18
Q

With ACEi measure VBG when?

A

3-14 days - increase by ≥30% of the baseline concentration creat. = AKI

19
Q

Spironolactone added at what stage and MoA:

A

2.0 mg/kg PO q12 ‐ 24 h Stage C heart failure

primary benefit is aldosterone antagonism

20
Q

define cardiac cachexia

A
  • loss of muscle or lean body mass associated with heart failure, with or without clinically relevant accompanying weight loss
  • negative prognostic implications and is much easier to prevent than to treat (Class I, LOE: moderate)
21
Q

Tx Stage D:

A

2 mg/kg IV bolus followed by either additional bolus doses or a furosemide CRI at a dosage of 0.66‐1 mg/kg/h
maximum of 4 hours. (Class I, LOE: expert opinion)

22
Q

Torsemide

Benefit

A

potent long‐acting loop diuretic used to treat dogs no longer adequately responsive to furosemide (0.1‐0.2 mg/kg q12h‐q24h or approximately 5%‐10% of the current furosemide dosage to deliver a furosemide‐equivalent dose)

diuresis induced by torsemide produces less renin‐angiotensin‐aldosterone system activation than more frequent doses of furosemide

23
Q

MV

A

mechanical ventilatory assistance may be useful in making the patient comfortable, in allowing time for medications to have an effect, and in providing time for left atrial dilatation to accommodate sudden increases in mitral valve regurgitant volume in patients with acute exacerbation of MMVD (eg, chordae tendineae rupture with severe cardiogenic pulmonary edema) and impending respiratory failure

24
Q

Stage D afterload reduction

A

CRI IV of sodium nitroprusside (for afterload reduction) or dobutamine (for inotropic support, especially in hypotensive patients) or both is recommended by a majority of panelists

Potentially beneficial PO drugs that decrease afterload in this situation include hydralazine (0.5‐2.0 mg/kg PO) with hourly dosage increases or amlodipine (approximately 0.05‐0.1 mg/kg PO, also to effect, although maximal drug effect does not occur for approximately 3 hours, mandating a slower titration).

25
Q

Stage D afterload reduction - should we be worried about plummeting BP?

A

The panel emphasized that because afterload reduction may increase cardiac output substantially in the setting of severe MR and heart failure, administration of an effective arterial dilator drug in this setting does not necessarily compromise blood pressure. (Class IIa, LOE: expert opinion).

26
Q

occurrence of ascites or jugular distension in patients with primarily left‐sided heart disease should prompt:

A

suggestive of pulmonary hypertension and should prompt an attempt to conclusively diagnose and identify patients that may benefit from sildenafil

27
Q

Stage D pimo:

A

Pimobendan dosage may be increased (off‐label use) to include a third 0.3 mg/kg daily PO dose (ie, 0.3 mg/kg PO q8h)
owner consent b/c off-label

28
Q

Stage D at home:

A

Furosemide or Torsemide

Spironolactone, if not already started as recommended in Stage C, is indicated for chronic treatment of Stage D patients

Hydrochlorothiazide was recommended by several panelists

Pimobendan dosage is increased by some panelists to include a third 0.3 mg/kg daily dose

Additional afterload reduction, using either amlodipine or hydralazine (see dosages and cautions above), may provide additional hemodynamic benefit and decrease cough frequency.

Digoxin, at the same (relatively low) dosages recommended by some panelists for Stage C heart failure with atrial fibrillation, is recommended for the treatment of atrial fibrillation in Stage D patients lacking a concrete contraindication.ith clinical signs related to exertion and in management of ascites when there is echocardiographic evid